terminology and guidelines for glaucoma ii - Kwaliteitskoepel

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$Refractiechirurgie - Nederlands Oogheelkundig Gezelschap$

2.4 - PRIMARY ANGLE-CLOSURE Primary angle-closure is appositional or synechial closure of the anterior chamber angle due to a number of possible mechanisms. This may result in raised IOP and may cause structural changes in the eye. The principal argument to strictly separate primary angle-closure glaucoma from primary open-angle glaucoma is the initial therapeutic approach (i.e. iridotomy or iridectomy) and the possible late complications (synechial closure of chamber angle) or the complications resulting when this type of glaucoma undergoes filtering surgery (uveal effusion, malignant glaucoma) 7,8 . Angle-closure glaucomas are clinically divided into the acute and chronic forms. The pathogenesis is however multifold and varies according to the underlying condition. By definition, in acute angle-closure, the chamber angle is closed by iridocorneal apposition that can be reversed, whereas in chronic angle-closure, the angle-closure is irreversible due to peripheral anterior synechiae. PROVOCATIVE TESTS In general provocative tests for angle-closure provide little additional information since even when negative they may not rule out the potential for angle-closure. In addition they may be hazardous, triggering an acute angle-closure attack even while the patient is monitored. 2.4.1 - PRIMARY ANGLE-CLOSURE (PAC) Angle-closure is defined on the basis of findings at gonioscopy Mechanisms of primary angle-closure 9,10 It is always important to exclude secondary causes of narrow or closed-angles such as a phakomorphic or inflammatory mechanism. In isometropic eyes this can be helped by comparing axial anterior chamber depths. A-scan or UBM may be helpful in defining the anatomical relationships and measure axial length, AC depth and lens thickness or PC configuration. In primary angle-closure these will be the same in each eye. a) Pupillary block mechanism A component of pupillary block accounts for most cases of acute, intermittent and chronic primary angle-closure. In pupillary block, the flow of aqueous from the posterior chamber through the pupil to the anterior chamber is impeded causing the pressure in the posterior chamber to become higher than the pressure in the anterior chamber. As a result, the peripheral iris, which is thinner than the central iris, bows forward and comes into contact with the trabecular meshwork and Schwalbe’s line. This circular obstruction of the trabecular outflow leads to a rise of IOP up to levels of 50-80 mm Hg; when this occurs within a few hours, it causes the symptoms and signs of acute angle-closure(AAC). The increased resistance to transpupillary aqueous flow is caused by apposition of the posterior surface of the iris to the anterior surface of the lens. The pupillary block mechanism may be precipitated during mid-dilation of the pupil or in conditions where the constrictor and dilator muscles of the pupil are acting together, physiologically as in reading in poor light or pharmacologically, such as with miotic therapy and concomitant dilator muscle stimulation by phenylephrine (the Mapstone provocation test) 5 . In most cases, the predisposition to pupil block is created by a narrow anterior segment and the agerelated increase of lens volume (see Ch. 2.5.1 and 2.5.3). The prevalence of PAC is higher in hyperopia, in elderly patients, in diabetics, women and in some races (especially Sino-Mongolians) 8,9 . Ch. 2 - 13 EGS
) Plateau-iris mechanism The isolated plateau iris mechanism causes angle-closure by direct obliteration of the chamber angle recess, crowded by the iris base when the pupil is dilated. This can occur only with one or more of the following: (1) the tissue of the peripheral iris is thick (iris rolls) (2) the iris base inserts anteriorly, leaving only a very narrow ciliary band, or inserts at the scleral spur (3) the ciliary processes are displaced anteriorly in the posterior chamber and push the iris base into the chamber angle. (4) the iris profile is almost flat from the perifery to the far periphery, where it becomes very steep, creating an extremely narrow angle recess. The iris root position and the posterior chamber anatomy can be confirmed by ultrasound biomicroscopy. It is clear from these descriptions why the isolated plateau iris mechanism is not altered by iridectomy. The pure plateau iris syndrome, causing angle-closure despite a patent iridotomy, is extremely rare compared with pupillary block. Both mechanisms, however, may coincide when “plateau iris configuration” is present. This latter condition is relatively common. The pure form of plateau iris syndrome can only be proven by the occurrence of acute angle-closure triggered by mydriasis despite a patent iridectomy and a centrally deep anterior chamber. Due to the above mechanisms, in all combined pupillary block/plateau iris cases iridotomy or iridectomy should be performed first. Plateau iris can be treated by argon laser iridoplasty and/or miotic therapy, preferably with topical sympatholytics like dapiprazole or thymoxamine. Strong miotics are to be avoided, because they cause anterior rotation of the ciliary body. Ideally, treatment should be instituted before synechial closure of the angle occurs (see Ch. 4.4.1). c) Lens mechanism Large and/or anteriorly placed cristalline lens can predispose per se to angle-closure and be a factor in worsening pupillary block. It can also cause secondary angle-closure glaucoma (see Ch. 2.5.1 and 2.5.3.). d) Creeping angle-closure mechanism Some cases of chronic angle-closure glaucoma result from synechial closure of the chamber angle, caused by a previous acute angle-closure ‘attack’, while creeping angle-closure is probably a primary event. The iris base ‘creeps’ on to the trabecular meshwork forming irreversible peripheral anterior synechiae (PAS). The IOP usually rises when more than half of the angle is obstructed. It is not yet clear whether creeping angle-closure is the consequence of undiagnosed intermittent angle-closure or a consequence of chronic miotic therapy causing worsening relative pupillary block. This form seems to be more frequent in Asians. e) Posterior aqueous misdirection mechanism In rare cases posterior aqueous misdirection can be the cause of primary angle-closure, mostly resulting in chronic IOP elevation. In these cases, usually younger or middle aged women, the ciliary processes come into contact with the lens equator, and/or a firm zonule/posterior capsule diaphragm, causing misdirection of aqueous into the vitreous 8,9 . As a consequence, the lens/iris diaphragm is pushed forward and occludes the chamber angle. Eyes predisposed to posterior aqueous misdirection often have narrow anterior chambers (peripheral and axial) and hypermetropia. After iridotomy or iridectomy, the use of miotics raises the IOP, whereas the use of cycloplegics reduces the IOP. This ‘inverse’ or ‘paradoxical’ reaction to parasympathomimetics should be tested only after iridotomy has been performed. Ultrasound biomicroscopy can demonstrate abnormal posterior chamber anatomy in these rare cases (see Ch. 2.5.3). Systemic drugs and angle-closure: Systemic drugs which may induce angle-closure in pre-disposed individuals are phenothiazines and their derivatives, tricyclic and non-tricyclic antidepressants, monoamine oxidase inhibitors, antihistamines, anti-Parkinson drugs, some minor tranquilizers, parasympatholytic and sympathomimetic agent (see Ch. 1.4). Ch. 2 - 14 EGS
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ISBN: 88-87434-13-1 Editrice DOGMA
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ACKNOWLEDGEMENT This work was made
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2.2.5 - Primary Open-Angle Glaucoma
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Foreword These Definitions and Guid
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INTRODUCTION The aim of the book is
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Since resources are limited worldwi
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II - RANDOMIZED CONTROLLED TRIALS F
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II.3 - COLLABORATIVE NORMAL TENSION
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No stratification for stage of dise
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II. 6. 3 - from CNTG 1. Therapy tha
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References 1) The Ocular Hypertensi
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I - QUESTIONS TO ASK TO YOUR GLAUCO
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III - ABNORMAL THRESHOLD VISUAL FIE
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V - GONIOSCOPIC OPEN ANGLES SOME DI
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VII - TREATMENT STEPLADDER JUVENILE
Page 32 and 33: IX - MONOTHERAPY (in alphabetic ord
Page 34 and 35: XI - MANAGEMENT ACUTE ANGLE CLOSURE
Page 36 and 37: XIII - ANTIMETABOLITES FOR WOUND MO
Page 38 and 39: CHAPTER 1 PATIENT EXAMINATION
Page 40 and 41: Other methods 22-25 : Air-puff tono
Page 42 and 43: References 1) Martin XD. Normal int
Page 44 and 45: 1.2 - GONIOSCOPY Gonioscopy is a fu
Page 46 and 47: 1 2 3 4 Fig. 1 Dynamic indentation
Page 48 and 49: The Spaeth classification Insertion
Page 50 and 51: References 1) Palmberg P. Gonioscop
Page 52 and 53: small - size mid - size large - siz
Page 54 and 55: Fig. 5 A) Cirumlinear vessel, B) Ba
Page 56 and 57: 1.3.4.3 - OCT The Optical Coherence
Page 58 and 59: 31) Carpineto P, Ciancaglini M, Zup
Page 60 and 61: central 24 or 30 central degrees re
Page 62 and 63: A retinal sensitivity value worse t
Page 64 and 65: HODAPP CLASSIFICATION 31 EARLY GLAU
Page 66 and 67: References 1) Bengtsson B, Heijl A,
Page 68 and 69: 1.5 - BLOOD FLOW 1.5.1 - VASCULAR F
Page 70 and 71: 28) Flammer J, Orgul S, Costa VP, O
Page 72 and 73: All forms of glaucoma should be cla
Page 74 and 75: 2.2 - PRIMARY OPEN-ANGLE GLAUCOMAS
Page 76 and 77: 2.2.4 - PRIMARY OPEN-ANGLE GLAUCOMA
Page 78 and 79: 2.3 - SECONDARY OPEN-ANGLE GLAUCOMA
Page 80 and 81: 2.3.1.6 - Glaucoma due to intraocul
Page 84 and 85: Systemic Risk factors for primary a
Page 86 and 87: OCCLUDABLE ANGLE: “Occludable”
Page 88 and 89: 2.5.3 - SECONDARY ANGLE-CLOSURE GLA
Page 90 and 91: CHAPTER 3 TREATMENT PRINCIPLES and
Page 92 and 93: Furthermore, blindness may occur de
Page 94 and 95: T A R G E T I O P Target IOP range
Page 96 and 97: Practical points for topical medica
Page 98 and 99: 3.3.1.1 - Category: ADRENERGIC AGON
Page 100 and 101: 3.3.1.2 - Category: ADRENERGIC ANTA
Page 102 and 103: 3.3.1.3 - Category: CARBONIC ANHYDR
Page 104 and 105: 3.3.1.4 - Category: PARASYMPATHOMIM
Page 106 and 107: 3.3.1.5 - Category: PROSTAGLANDIN D
Page 108 and 109: Drug interactions Precipitation occ
Page 110 and 111: COMBINATION THERAPY Starting* Addit
Page 112 and 113: 3.3.2.2 - Category: ADRENERGIC ANTA
Page 114 and 115: Pregnancy and nursing mothers Only
Page 116 and 117: 3.5 - LASER SURGERY 3.5.1 - LASER I
Page 118 and 119: 3.5.2 - LASER TRABECULOPLASTY 77-89
Page 120 and 121: 3.5.4 - CYCLOPHOTOCOAGULATION Indic
Page 122 and 123: Although medical therapy is still t
Page 124 and 125: 3.6.4 - COMPLEX CASES Complicated g
Page 126 and 127: Post-operative use Concentration: 0
Page 128 and 129: 25) Janz NK, Wren PA, Lichter PR, M
Page 130 and 131: (Rescula TM ) in patients with glau
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in white patients with open-angle g
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CHAPTER 4 TREATMENT GUIDELINES
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4.2 - PRIMARY OPEN-ANGLE GLAUCOMAS
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4.2.7 - OCULAR HYPERTENSION (OH) Al
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4.3.1.7 - Glaucoma associated with
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• Withdrawal of aqueous from vitr
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4.5 - SECONDARY ANGLE-CLOSURE GLAUC
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4.5.3 - SECONDARY ANGLE-CLOSURE GLA
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NOTES
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NOTES
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NOTES
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